FUSE binding protein FUBP3 is a potent regulator in Japanese encephalitis virus infection

Abstract Background The JEV genome is a positive-sense RNA with a highly structured capped 5′UTR, 3′UTR and a large open reading frame. 3′UTR is the untranslated region of flavivirus and has various important functions during viral replication, such as translation, replication and encapsidation. Dur...

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Autores principales:	Peng Xu, Wei Tong, Young-Mao Chen
Formato:	article
Lenguaje:	EN
Publicado:	BMC 2021
Materias:	Japanese encephalitis virus Far upstream element-binding protein 3 Untranslated region Viral replication Infectious and parasitic diseases RC109-216
Acceso en línea:	https://doaj.org/article/2a2fbdb987fe43a08eaa647cd3f97443
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spelling	oai:doaj.org-article:2a2fbdb987fe43a08eaa647cd3f974432021-11-21T12:02:10ZFUSE binding protein FUBP3 is a potent regulator in Japanese encephalitis virus infection10.1186/s12985-021-01697-81743-422Xhttps://doaj.org/article/2a2fbdb987fe43a08eaa647cd3f974432021-11-01T00:00:00Zhttps://doi.org/10.1186/s12985-021-01697-8https://doaj.org/toc/1743-422XAbstract Background The JEV genome is a positive-sense RNA with a highly structured capped 5′UTR, 3′UTR and a large open reading frame. 3′UTR is the untranslated region of flavivirus and has various important functions during viral replication, such as translation, replication and encapsidation. During viral replication, the 3′UTR interacts with viral proteins and host proteins and is required for viral RNA replication and translocation. Methods The expression level of FUBP3 was knocked down by siRNA and Flag-tagged FUBP3 overexpression plasmid was constructed for overexpression. BHK-21 cells were cultured and infected with JEV to investigate the functional role of FUBP3 in the viral infection cycle. Subcellular localization of FUBP3 and viral replication complexes was observed by dual immunofluorescence staining. Results Four host proteins were specifically associated with the 3′UTR of JEV, and FUBP3 was selected to further investigate its potential functional role in the JEV infection cycle. Knockdown of FUBP3 protein resulted in a significant decrease in JEV viral titer, whereas ectopic overexpression of FUBP3 resulted in increased JE viral infectivity. In cells stably knocked down for FUBP3 and then infected with JEV, we found almost no detectable viral NS5 protein. In contrast, when cells stably knocking-down of FUBP3 overexpressed FUBP3, we found a significant increase in viral RNA production over time compared to controls. We also demonstrated that FUBP3 re-localized in the cytoplasm after infection with JEV and co-localized with viral proteins. Exogenous overexpression of FUBP3 was also shown to be located in the JE replication complex and to assist viral replication after JEV infection. Conclusions The overall results suggest that FUBP3 regulates RNA replication of JEV and promotes subsequent viral translation and viral particle production.Peng XuWei TongYoung-Mao ChenBMCarticleJapanese encephalitis virusFar upstream element-binding protein 3Untranslated regionViral replicationInfectious and parasitic diseasesRC109-216ENVirology Journal, Vol 18, Iss 1, Pp 1-11 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Japanese encephalitis virus Far upstream element-binding protein 3 Untranslated region Viral replication Infectious and parasitic diseases RC109-216
spellingShingle	Japanese encephalitis virus Far upstream element-binding protein 3 Untranslated region Viral replication Infectious and parasitic diseases RC109-216 Peng Xu Wei Tong Young-Mao Chen FUSE binding protein FUBP3 is a potent regulator in Japanese encephalitis virus infection
description	Abstract Background The JEV genome is a positive-sense RNA with a highly structured capped 5′UTR, 3′UTR and a large open reading frame. 3′UTR is the untranslated region of flavivirus and has various important functions during viral replication, such as translation, replication and encapsidation. During viral replication, the 3′UTR interacts with viral proteins and host proteins and is required for viral RNA replication and translocation. Methods The expression level of FUBP3 was knocked down by siRNA and Flag-tagged FUBP3 overexpression plasmid was constructed for overexpression. BHK-21 cells were cultured and infected with JEV to investigate the functional role of FUBP3 in the viral infection cycle. Subcellular localization of FUBP3 and viral replication complexes was observed by dual immunofluorescence staining. Results Four host proteins were specifically associated with the 3′UTR of JEV, and FUBP3 was selected to further investigate its potential functional role in the JEV infection cycle. Knockdown of FUBP3 protein resulted in a significant decrease in JEV viral titer, whereas ectopic overexpression of FUBP3 resulted in increased JE viral infectivity. In cells stably knocked down for FUBP3 and then infected with JEV, we found almost no detectable viral NS5 protein. In contrast, when cells stably knocking-down of FUBP3 overexpressed FUBP3, we found a significant increase in viral RNA production over time compared to controls. We also demonstrated that FUBP3 re-localized in the cytoplasm after infection with JEV and co-localized with viral proteins. Exogenous overexpression of FUBP3 was also shown to be located in the JE replication complex and to assist viral replication after JEV infection. Conclusions The overall results suggest that FUBP3 regulates RNA replication of JEV and promotes subsequent viral translation and viral particle production.
format	article
author	Peng Xu Wei Tong Young-Mao Chen
author_facet	Peng Xu Wei Tong Young-Mao Chen
author_sort	Peng Xu
title	FUSE binding protein FUBP3 is a potent regulator in Japanese encephalitis virus infection
title_short	FUSE binding protein FUBP3 is a potent regulator in Japanese encephalitis virus infection
title_full	FUSE binding protein FUBP3 is a potent regulator in Japanese encephalitis virus infection
title_fullStr	FUSE binding protein FUBP3 is a potent regulator in Japanese encephalitis virus infection
title_full_unstemmed	FUSE binding protein FUBP3 is a potent regulator in Japanese encephalitis virus infection
title_sort	fuse binding protein fubp3 is a potent regulator in japanese encephalitis virus infection
publisher	BMC
publishDate	2021
url	https://doaj.org/article/2a2fbdb987fe43a08eaa647cd3f97443
work_keys_str_mv	AT pengxu fusebindingproteinfubp3isapotentregulatorinjapaneseencephalitisvirusinfection AT weitong fusebindingproteinfubp3isapotentregulatorinjapaneseencephalitisvirusinfection AT youngmaochen fusebindingproteinfubp3isapotentregulatorinjapaneseencephalitisvirusinfection
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FUSE binding protein FUBP3 is a potent regulator in Japanese encephalitis virus infection

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